Zhu Yongwen, Lu Lin, Liao Xiudong, Li Wenxiang, Zhang Liyang, Ji Cheng, Lin Xi, Liu Hsiao-Ching, Odle Jack, Luo Xugang
Mineral Nutrition Research Division, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
College of Animal Science, South China Agricultural University, Guangzhou 510000, China.
Oncotarget. 2017 Sep 11;8(52):89665-89680. doi: 10.18632/oncotarget.20804. eCollection 2017 Oct 27.
Maternal heat stress induced the aberrant epigenetic patterns resulting in the abnormal development of offspring embryos. It is unclear whether maternal dietary manganese supplementation as an epigenetic modifier could protect the chick embryonic development against maternal heat stress via epigenetic mechanisms. To test this hypothesis using an avian model, a completely randomized design with a 2 (maternal normal and high environmental temperatures of 21 and 32°C, respectively) × 3 (maternal dietary manganese sources, the control diet without manganese supplementation and the control diet + 120 mg/kg as either inorganic or organic manganese) factorial arrangement was adopted. Maternal environmental hyperthermia increased mRNA expressions of heat shock proteins 90 and 70, cyclin-dependent kinase 6 and B-cell CLL/lymphoma 2-associated X protein displaying oxidative damage and apoptosis in the embryonic heart. Maternal environmental hyperthermia impaired the embryonic development associated with the alteration of epigenetic status, as evidenced by global DNA hypomethylation and histone 3 lysine 9 hypoacetylation in the embryonic heart. Maternal dietary manganese supplementation increased the heart anti-apoptotic gene B-cell CLL/lymphoma 2 expressions under maternal environmental hyperthermia and manganese superoxide dismutase enzyme activity in the embryonic heart. Maternal dietary organic Mn supplementation effectively eliminated the impairment of maternal environmental hyperthermia on the embryonic development. Maternal dietary manganese supplementation up-regulated manganese superoxide dismutase mRNA expression by reducing DNA methylation and increasing histone 3 lysine 9 acetylation of its promoter. It is suggested that maternal dietary manganese addition could protect the chick embryonic development against maternal heat stress via enhancing epigenetic-activated antioxidant and anti-apoptotic abilities.
母体热应激会诱导异常的表观遗传模式，导致后代胚胎发育异常。目前尚不清楚作为表观遗传修饰剂的母体膳食锰补充是否能通过表观遗传机制保护鸡胚发育免受母体热应激的影响。为了使用禽类模型验证这一假设，采用了完全随机设计，有2（母体正常和高温环境温度分别为21和32°C）×3（母体膳食锰来源，不添加锰的对照日粮和添加120 mg/kg无机或有机锰的对照日粮）的析因安排。母体环境高温会增加热休克蛋白90和70、细胞周期蛋白依赖性激酶6以及B细胞淋巴瘤/白血病-2相关X蛋白的mRNA表达，这些蛋白在胚胎心脏中表现出氧化损伤和凋亡。母体环境高温会损害与表观遗传状态改变相关的胚胎发育，胚胎心脏中的全基因组DNA低甲基化和组蛋白3赖氨酸9低乙酰化证明了这一点。母体膳食锰补充会增加母体环境高温下心脏抗凋亡基因B细胞淋巴瘤/白血病-2的表达以及胚胎心脏中的锰超氧化物歧化酶活性。母体膳食有机锰补充有效消除了母体环境高温对胚胎发育的损害。母体膳食锰补充通过降低DNA甲基化并增加其启动子的组蛋白3赖氨酸9乙酰化来上调锰超氧化物歧化酶mRNA表达。研究表明，母体膳食添加锰可以通过增强表观遗传激活的抗氧化和抗凋亡能力来保护鸡胚发育免受母体热应激的影响。
